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Pharma2 MCQs > أسئلة ضع دائرة على السكري > Flashcards

أسئلة ضع دائرة على السكري Flashcards

1
Q

Which hormone is produced by β cells in the pancreas?
a. Glucagon
b. Somatostatin
c. Insulin
d. Amylin

A

c. Insulin

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2
Q

Which cells in the pancreas are responsible for producing glucagon?
a. β cells
b. α cells
c. δ cells
d. PP cells

A

b. α cells

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3
Q

Somatostatin is produced by which type of cells in the pancreas?
a. β cells
b. α cells
c. δ cells
d. PP cells

A

c. δ cells

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4
Q

What condition is caused by a lack of insulin?
a. Hypoglycemia
b. Severe hyperglycemia
c. Hyperthyroidism
d. Hypothyroidism

A

b. Severe hyperglycemia

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5
Q

Untreated severe hyperglycemia can lead to which of the following complications?
a. Retinopathy
b. Nephropathy
c. Neuropathy
d. All of the above

A

d. All of the above

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6
Q

How many people worldwide are affected by diabetes?
a. 100 million
b. 150 million
c. 180 million
d. 200 million

A

c. 180 million

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7
Q

Diabetes is best described as:
a. A single disease
b. A group of heterogeneous syndromes
c. A viral infection
d. A bacterial infection

A

b. A group of heterogeneous syndromes

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8
Q

Which of the following is NOT a clinical classification of diabetes?
a. Type 3: insulin-resistant
b. Type 1: insulin-dependent
c. Type 2: non-insulin-dependent
d. Gestational diabetes

A

a. Type 3: insulin-resistant

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9
Q

Gestational diabetes affects which group of people?
a. Elderly
b. Teenagers
c. Pregnant women
d. Infants

A

c. Pregnant women

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10
Q

Diabetes due to other factors can be caused by:
a. Viral infections
b. Genetics or medication
c. Poor diet
d. Lack of exercise

A

b. Genetics or medication

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11
Q

Type 1 diabetes most commonly affects individuals in:
a. Infancy
b. Puberty or early adulthood
c. Middle age
d. Old age

A

b. Puberty or early adulthood

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12
Q

What is the cause of absolute insulin deficiency in type 1 diabetes?
a. Insulin resistance
b. Massive β-cell necrosis
c. Decreased insulin production
d. Increased glucagon production

A

b. Massive β-cell necrosis

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13
Q

The autoimmune process in type 1 diabetes is directed against which cells?
a. α cells
b. δ cells
c. β cells
d. PP cells

A

c. β cells

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14
Q

Which of the following are symptoms of type 1 diabetes?
a. Polydipsia, polyuria, and weight loss
b. Hyperactivity, weight gain, and hypertension
c. Hypoglycemia, fatigue, and muscle cramps
d. Fever, chills, and headaches

A

a. Polydipsia, polyuria, and weight loss

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15
Q

What life-threatening condition is associated with type 1 diabetes?
a. Hyperglycemic hyperosmolar syndrome
b. Ketoacidosis
c. Hypoglycemia
d. Diabetic foot

A

b. Ketoacidosis

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16
Q

To control hyperglycemia and ketoacidosis in type 1 diabetes, what is required?
a. Oral hypoglycemic agents
b. Exogenous insulin
c. Dietary modifications only
d. Exercise only

A

b. Exogenous insulin

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17
Q

Maintaining the accepted level of glycosylated hemoglobin (HbA1c) helps to avoid:
a. Hypoglycemia
b. Hyperthyroidism
c. Long term complications
d. Hypertension

A

c. Long term complications

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18
Q

Individuals with type 1 diabetes cannot maintain normal levels of which hormone?
a. Glucagon
b. Somatostatin
c. Insulin
d. Cortisol

A

c. Insulin

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19
Q

What type of diabetes is most common?
a. Type 2
b. Type 1
c. Gestational diabetes
d. MODY (Maturity Onset Diabetes of the Young)

A

a. Type 2

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20
Q

Which factors influence the development of type 2 diabetes?
a. Viral infections
b. Genetic factors, aging, obesity, and peripheral insulin resistance
c. Lack of physical activity
d. Excessive sugar intake

A

b. Genetic factors, aging, obesity, and peripheral insulin resistance

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21
Q

Type 2 diabetes is characterized by:
a. Severe metabolic alterations
b. Milder metabolic alterations than type 1
c. Ketoacidosis
d. Complete loss of β-cell function

A

b. Milder metabolic alterations than type 1

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22
Q

In type 2 diabetes, what happens to β-cell function over time?
a. It remains constant
b. It improves
c. It declines
d. It completely stops

A

c. It declines

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23
Q

What is the major cause of type 2 diabetes?
a. Excessive insulin production
b. Lack of sensitivity of target organs to insulin
c. Autoimmune destruction of β-cells
d. Increased glucagon production

A

b. Lack of sensitivity of target organs to insulin

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24
Q

Which of the following is NOT a characteristic of type 2 diabetes?
a. Ketoacidosis
b. Retention of some β-cell function
c. Variable insulin secretion
d. Gradual reduction in β-cell mass

A

a. Ketoacidosis

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25
Q

The treatment for type 2 diabetes primarily aims to:
a. Increase insulin production
b. Induce weight loss
c. Prevent long-term complications
d. Enhance glucose absorption

A

c. Prevent long-term complications

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26
Q

As type 2 diabetes progresses, what is often required to maintain satisfactory serum glucose levels?
a. Increased physical activity
b. Insulin therapy
c. Reduced carbohydrate intake
d. Increased protein intake

A

b. Insulin therapy

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27
Q

Why is insulin administered by subcutaneous injection?
a. It is degraded in the GIT if taken orally
b. It is more effective when injected
c. It causes less pain
d. It has a longer duration of action

A

a. It is degraded in the GIT if taken orally

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28
Q

Insulin is synthesized as which precursor?
a. Pre-insulin
b. Pro-insulin
c. Pre-pro-insulin
d. Insulinogen

A

b. Pro-insulin

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29
Q

The process that converts pro-insulin to insulin involves:
a. Proteolytic cleavage
b. Hydrolysis
c. Oxidation
d. Phosphorylation

A

a. Proteolytic cleavage

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30
Q

Which cells secrete insulin and C peptide?
a. α cells
b. δ cells
c. β cells
d. PP cells

A

c. β cells

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31
Q

Measurement of which peptide provides a better index of insulin levels?
a. Insulin
b. C peptide
c. Glucagon
d. Amylin

A

b. C peptide

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32
Q

What is the most important regulator of insulin secretion?
a. Blood glucose
b. Certain amino acids
c. Gastrointestinal hormones
d. Autonomic mediators

A

a. Blood glucose

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33
Q

Which of the following also regulates insulin secretion?
a. Blood pressure
b. Blood pH
c. Certain amino acids
d. Blood oxygen levels

A

c. Certain amino acids

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34
Q

Insulin secretion is influenced by gastrointestinal hormones and:
a. Blood cholesterol
b. Autonomic mediators
c. Plasma proteins
d. Blood calcium levels

A

b. Autonomic mediators

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35
Q

What enzyme phosphorylates glucose in the pancreas?
a. Hexokinase
b. Glucokinase
c. Phosphofructokinase
d. Glucose-6-phosphatase

A

b. Glucokinase

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36
Q

The phosphorylation of glucose in the pancreas leads to the production of:
a. ADP
b. AMP
c. ATP
d. GTP

A

c. ATP

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37
Q

ATP production in the pancreas inhibits the efflux of which ion?
a. Sodium (Na+)
b. Potassium (K+)
c. Calcium (Ca++)
d. Chloride (Cl-)

A

b. Potassium (K+)

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38
Q

The inhibition of K+ efflux causes what cellular event?
a. Hyperpolarization
b. Depolarization
c. Repolarization
d. Hypopolarization

A

b. Depolarization

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39
Q

The increased intracellular concentration of which ion stimulates insulin secretion?
a. Sodium (Na+)
b. Calcium (Ca++)
c. Potassium (K+)
d. Chloride (Cl-)

A

b. Calcium (Ca++)

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40
Q

Which process results in the direct secretion of insulin?
a. Inhibition of ATP production
b. Hyperpolarization of pancreatic cells
c. Decreased intracellular calcium levels
d. Depolarization of pancreatic cells leading to increased intracellular calcium levels

A

d. Depolarization of pancreatic cells leading to increased intracellular calcium levels

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41
Q

The variation in the times of onset and durations of activity of insulin preparations is primarily due to:
a. Differences in the amino acid sequences of the polypeptides and the type of formulation
b. The source of insulin
c. The dosage of insulin
d. The route of administration

A

a. Differences in the amino acid sequences of the polypeptides and the type of formulation

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42
Q

Which of the following insulins have a faster onset and shorter duration of action than regular insulin?
a. Glargine and detemir
b. Lispro, aspart, and glulisine
c. NPH and regular insulin
d. Lente and ultralente

A

b. Lispro, aspart, and glulisine

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43
Q

Why do insulins like lispro, aspart, and glulisine have a faster onset of action?
a. They are administered orally
b. They are more potent
c. They do not aggregate or form complexes
d. They have a higher concentration

A

c. They do not aggregate or form complexes

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44
Q

Which insulins are classified as long-acting and show prolonged, flat levels of the hormone following injection?
a. Glargine and detemir
b. Lispro and aspart
c. Regular and NPH
d. Lente and ultralente

A

a. Glargine and detemir

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45
Q

What characteristic of glargine and detemir makes them suitable as long-acting insulins?
a. They are rapidly absorbed
b. They have prolonged, flat levels of the hormone
c. They are taken orally
d. They are mixed with other insulins

A

b. They have prolonged, flat levels of the hormone

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46
Q

What is the most serious and common adverse reaction to an overdose of insulin?
a. Weight gain
b. Lipodystrophy
c. Hypoglycemia
d. Allergic reactions

A

c. Hypoglycemia

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47
Q

Which of the following is a possible adverse reaction to insulin?
a. Hair loss
b. Muscle cramps
c. Weight gain
d. Hyperglycemia

A

c. Weight gain

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48
Q

Which adverse reaction to insulin is less common with human insulin?
a. Hypoglycemia
b. Lipodystrophy
c. Weight gain
d. Allergic reactions

A

b. Lipodystrophy

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49
Q

Adverse reactions to insulin can include:
a. Allergic reactions and local injection site reactions
b. Increased appetite and sweating
c. Dehydration and dry skin
d. Fever and chills

A

a. Allergic reactions and local injection site reactions

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50
Q

Hypoglycemia caused by an insulin overdose is considered:
a. Mild and rare
b. The most serious and common adverse reaction
c. Temporary and harmless
d. Unrelated to insulin dosage

A

b. The most serious and common adverse reaction

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51
Q

Which of the following is a type of rapid-acting insulin preparation?
a. Insulin glargine
b. Insulin lispro
c. NPH insulin
d. Insulin detemir

A

b. Insulin lispro

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52
Q

Which insulin can be given intravenously in emergencies?
a. Regular insulin
b. Insulin aspart
c. Insulin glulisine
d. Insulin lispro

A

a. Regular insulin

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53
Q

What is the pregnancy category for rapid-acting and short-acting insulin preparations?
a. Category B
b. Category A
c. Category C
d. Category D

A

a. Category B

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54
Q

Rapid-acting insulin preparations are usually administered:
a. Once a day in the morning
b. At bedtime
c. Immediately before or following a meal
d. Once a week

A

c. Immediately before or following a meal

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55
Q

Why are rapid-acting insulins like lispro, aspart, and glulisine used?
a. To replace basal insulin
b. To mimic the prandial (mealtime) release of insulin
c. To treat diabetic ketoacidosis
d. To manage long-term glucose control

A

b. To mimic the prandial (mealtime) release of insulin

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56
Q

What is the primary action of rapid-acting insulin preparations?
a. Rapidly lowers blood glucose
b. Slowly decreases blood glucose
c. Increases blood glucose
d. Stabilizes blood glucose levels

A

a. Rapidly lowers blood glucose

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57
Q

Rapid-acting insulin preparations are often used in combination with:
a. Oral hypoglycemic agents
b. Longer-acting insulins
c. Dietary supplements
d. Exercise regimens

A

b. Longer-acting insulins

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58
Q

What characteristic allows insulin lispro to act more rapidly after subcutaneous injection compared to regular insulin?
a. Higher potency
b. More rapid absorption
c. Longer duration of action
d. Delayed onset of action

A

b. More rapid absorption

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59
Q

What is another name for Neutral Protamine Hagedorn (NPH) insulin?
a. Insulin lispro
b. Insulin glulisine
c. Insulin glargine
d. Insulin isophane

A

d. Insulin isophane

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60
Q

NPH insulin should only be given:
a. Intravenously
b. Subcutaneously
c. Orally
d. Intramuscularly

A

b. Subcutaneously

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61
Q

NPH insulin is classified as:
a. Rapid-acting insulin
b. Short-acting insulin
c. Intermediate-acting insulin
d. Long-acting insulin

A

c. Intermediate-acting insulin

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62
Q

NPH insulin forms a less-soluble complex due to the presence of:
a. Zinc
b. Protamine
c. Albumin
d. Phosphate

A

b. Protamine

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63
Q

The delayed absorption of NPH insulin is caused by:
a. Increased solubility
b. Rapid metabolism
c. Formation of a less-soluble complex
d. Higher concentration of insulin

A

c. Formation of a less-soluble complex

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64
Q

The duration of action of NPH insulin is considered:
a. Short
b. Intermediate
c. Long
d. Ultra-long

A

b. Intermediate

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65
Q

What pH level does NPH insulin have?
a. Acidic
b. Basic
c. Neutral
d. Alkaline

A

c. Neutral

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66
Q

Which of the following statements about NPH insulin is true?
a. It can be given intravenously in emergencies
b. It is rapidly absorbed
c. It should never be given intravenously
d. It is a long-acting insulin

A

c. It should never be given intravenously

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67
Q

Intermediate-acting insulin is useful in treating all forms of diabetes except:
a. Type 1 diabetes
b. Type 2 diabetes
c. Diabetic ketoacidosis or emergency hyperglycemia
d. Gestational diabetes

A

c. Diabetic ketoacidosis or emergency hyperglycemia

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68
Q

Intermediate-acting insulin is usually given along with:
a. Long-acting insulin
b. Oral hypoglycemic agents
c. Rapid- or short-acting insulin
d. Dietary supplements

A

c. Rapid- or short-acting insulin

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69
Q

What is the role of intermediate-acting insulin in diabetes management?
a. To treat hypoglycemia
b. To provide basal insulin coverage
c. To manage acute hyperglycemia
d. To replace rapid-acting insulin

A

b. To provide basal insulin coverage

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70
Q

Neutral protamine lispro (NPL) insulin is used only in combination with:
a. Insulin glargine
b. Insulin detemir
c. Insulin lispro
d. Regular insulin

A

c. Insulin lispro

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71
Q

Which of the following is a premixed combination of human insulins?
a. 100% NPH insulin
b. 70% NPH insulin plus 30% regular insulin
c. 50% NPH insulin plus 50% insulin glulisine
d. 75% insulin glargine plus 25% insulin lispro

A

b. 70% NPH insulin plus 30% regular insulin

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72
Q

What is the purpose of using premixed combinations of human insulins?
a. To treat diabetic ketoacidosis
b. To provide both basal and prandial insulin coverage
c. To manage insulin resistance
d. To reduce insulin dosage

A

b. To provide both basal and prandial insulin coverage

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73
Q

What is the isoelectric point of insulin glargine compared to human insulin?
a. Higher
b. Lower
c. The same
d. Variable

A

b. Lower

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74
Q

The lower isoelectric point of insulin glargine leads to what at the injection site?
a. Precipitation, thereby extending its action
b. Rapid absorption
c. Immediate release
d. Decreased efficacy

A

a. Precipitation, thereby extending its action

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75
Q

Compared to NPH insulin, insulin glargine has a:
a. Faster onset
b. Slower onset
c. Similar onset
d. Variable onset

A

b. Slower onset

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76
Q

Insulin glargine is characterized by:
a. A rapid peak
b. No peak (flat)
c. Multiple peaks
d. Irregular peaks

A

b. No peak (flat)

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77
Q

Insulin glargine must be administered:
a. Orally
b. Intravenously
c. Intramuscularly
d. Subcutaneously

A

d. Subcutaneously

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78
Q

What type of hypoglycemic effect is associated with insulin glargine?
a. Short-acting
b. Prolonged hypoglycemic
c. Immediate
d. Variable

A

b. Prolonged hypoglycemic

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79
Q

Insulin glargine’s action is extended due to:
a. Increased solubility
b. Precipitation at the injection site
c. Rapid metabolism
d. Increased dosage

A

b. Precipitation at the injection site

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80
Q

The administration route of insulin glargine is primarily:
a. Oral
b. Intravenous
c. Subcutaneous
d. Intramuscular

A

c. Subcutaneous

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81
Q

Insulin detemir has a fatty-acid side chain that enhances its association with which protein?
a. Hemoglobin
b. Myoglobin
c. Albumin
d. Fibrinogen

A

c. Albumin

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82
Q

The slow dissociation from albumin results in which property of insulin detemir?
a. Rapid-acting
b. Long-acting
c. Intermediate-acting
d. Short-acting

A

b. Long-acting

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83
Q

Which insulin has similar long-acting properties to insulin detemir due to its slow dissociation from albumin?
a. Insulin lispro
b. Insulin aspart
c. Insulin glulisine
d. Insulin glargine

A

d. Insulin glargine

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84
Q

The enhanced association of insulin detemir with albumin is due to:
a. Increased solubility
b. Higher concentration
c. Fatty-acid side chain
d. Protein binding

A

c. Fatty-acid side chain

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85
Q

Which characteristic of insulin detemir allows it to have prolonged effects similar to insulin glargine?
a. Rapid absorption
b. Immediate release
c. Slow dissociation from albumin
d. High potency

A

c. Slow dissociation from albumin

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86
Q

Insulin detemir is classified as which type of insulin preparation?
a. Rapid-acting
b. Short-acting
c. Long-acting
d. Intermediate-acting

A

c. Long-acting

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87
Q

The fatty-acid side chain in insulin detemir contributes to:
a. Faster onset of action
b. Reduced potency
c. Enhanced association with albumin
d. Increased degradation

A

c. Enhanced association with albumin

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88
Q

The prolonged action of insulin detemir is mainly due to:
a. Slow dissociation from albumin
b. Fast absorption
c. High dosage
d. Rapid metabolism

A

a. Slow dissociation from albumin

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89
Q

Pramlintide is a synthetic analog of:
a. Amylin
b. Insulin
c. Glucagon
d. Somatostatin

A

a. Amylin

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90
Q

Pramlintide is indicated as an adjunct to which type of insulin therapy?
a. Basal insulin therapy
b. Mealtime insulin therapy
c. Long-acting insulin therapy
d. Intermediate-acting insulin therapy

A

b. Mealtime insulin therapy

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91
Q

Which of the following is an effect of pramlintide?
a. Increases gastric emptying
b. Delays gastric emptying
c. Increases postprandial glucagon secretion
d. Decreases insulin sensitivity

A

b. Delays gastric emptying

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92
Q

Pramlintide helps to decrease which of the following?
a. Insulin production
b. Postprandial glucagon secretion
c. Blood pressure
d. Cholesterol levels

A

b. Postprandial glucagon secretion

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93
Q

How is pramlintide administered?
a. Orally
b. Intravenously
c. Intramuscularly
d. Subcutaneously

A

d. Subcutaneously

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94
Q

When should pramlintide be injected?
a. Once a day in the morning
b. At bedtime
c. Immediately after meals
d. Immediately prior to meals

A

d. Immediately prior to meals

95
Q

Pramlintide is used in the management of which types of diabetes?
a. Type 1 diabetes only
b. Type 2 diabetes only
c. Both Type 1 and Type 2 diabetes
d. Gestational diabetes

A

c. Both Type 1 and Type 2 diabetes

96
Q

Which of the following statements is true about pramlintide?
a. It increases postprandial glucagon secretion
b. It is administered intravenously
c. It delays gastric emptying
d. It is not indicated for use with mealtime insulin

A

c. It delays gastric emptying

97
Q

When initiating pramlintide, the dose of rapid- or short-acting insulin should be decreased by:
a. 25%
b. 50%
c. 75%
d. 100%

A

b. 50%

98
Q

Why should the dose of rapid- or short-acting insulin be decreased when starting pramlintide?
a. To avoid a risk of severe hypoglycemia
b. To increase insulin effectiveness
c. To prevent hyperglycemia
d. To reduce gastrointestinal side effects

A

a. To avoid a risk of severe hypoglycemia

99
Q

The adverse effects of pramlintide are mainly:
a. Neurological
b. Cardiovascular
c. Gastrointestinal
d. Respiratory

A

c. Gastrointestinal

100
Q

Which of the following is NOT a common adverse effect of pramlintide?
a. Nausea
b. Anorexia
c. Hyperglycemia
d. Vomiting

A

c. Hyperglycemia

101
Q

Pramlintide should not be given to patients with:
a. Hypertension
b. Hyperlipidemia
c. Diabetic gastroparesis
d. Osteoporosis

A

c. Diabetic gastroparesis

102
Q

Pramlintide should be avoided in patients with a history of:
a. Hyperglycemia
b. Hypothyroidism
c. Hypoglycemic unawareness
d. Hypercalcemia

A

c. Hypoglycemic unawareness

103
Q

The main reason for avoiding pramlintide in patients with diabetic gastroparesis is:
a. Increased blood pressure
b. Delayed stomach emptying
c. Increased insulin secretion
d. Decreased insulin sensitivity

A

b. Delayed stomach emptying

104
Q

Pramlintide is administered to manage which condition?
a. Hypertension
b. Hyperlipidemia
c. Diabetes
d. Osteoporosis

A

c. Diabetes

105
Q

Sulfonylureas promote the release of insulin from which cells of the pancreas?
a. α cells
b. β cells
c. δ cells
d. PP cells

A

b. β cells

106
Q

What is one of the mechanisms of action of sulfonylureas?
a. Inhibition of insulin release
b. Stimulation of insulin release by blocking ATP-sensitive K+ channels
c. Decrease in peripheral insulin sensitivity
d. Increase in hepatic glucose production

A

b. Stimulation of insulin release by blocking ATP-sensitive K+ channels

107
Q

Blocking ATP-sensitive K+ channels by sulfonylureas leads to:
a. Hyperpolarization
b. Depolarization and Ca2+ influx
c. Decreased calcium levels
d. Reduced insulin secretion

A

b. Depolarization and Ca2+ influx

108
Q

Sulfonylureas may cause which of the following side effects?
a. Hyperglycemia
b. Hypoglycemia
c. Hyperkalemia
d. Hypokalemia

A

b. Hypoglycemia

109
Q

Which of the following is an additional action of sulfonylureas?
a. Increase in hepatic glucose production
b. Reduction in hepatic glucose production
c. Increase in insulin degradation
d. Inhibition of gluconeogenesis

A

b. Reduction in hepatic glucose production

110
Q

Sulfonylureas also contribute to diabetes management by:
a. Decreasing insulin sensitivity
b. Inhibiting insulin receptors
c. Increasing peripheral insulin sensitivity
d. Reducing glucose uptake

A

c. Increasing peripheral insulin sensitivity

111
Q

What is the result of increased peripheral insulin sensitivity due to sulfonylureas?
a. Enhanced glucose uptake by tissues
b. Decreased glucose uptake by tissues
c. Increased insulin resistance
d. Reduced insulin secretion

A

a. Enhanced glucose uptake by tissues

112
Q

Which channels are blocked by sulfonylureas to stimulate insulin release?
a. Sodium (Na+) channels
b. ATP-sensitive potassium (K+) channels
c. Calcium (Ca2+) channels
d. Chloride (Cl-) channels

A

b. ATP-sensitive potassium (K+) channels

113
Q

Which of the following is a first-generation sulfonylurea with the shortest action?
a. Tolbutamide
b. Glyburide
c. Glipizide
d. Glimepiride

A

a. Tolbutamide

114
Q

Which generation of sulfonylurea derivatives has a longer duration of action?
a. First generation
b. Second generation
c. Third generation
d. Fourth generation

A

b. Second generation

115
Q

Which second-generation sulfonylurea is considered a reasonably safe alternative to insulin therapy for diabetes in pregnancy?
a. Tolbutamide
b. Glyburide
c. Glipizide
d. Glimepiride

A

b. Glyburide

116
Q

Which of the following is NOT a second-generation sulfonylurea?
a. Glyburide
b. Glipizide
c. Tolbutamide
d. Glimepiride

A

c. Tolbutamide

117
Q

Which second-generation sulfonylurea is used for its longer duration of action?
a. Tolbutamide
b. Regular insulin
c. Glimepiride
d. NPH insulin

A

c. Glimepiride

118
Q

What is a characteristic of second-generation sulfonylureas compared to first-generation?
a. Longer duration of action
b. Shorter duration of action
c. Reduced efficacy
d. Increased side effects

A

a. Longer duration of action

119
Q

Glipizide belongs to which class of antidiabetic drugs?
a. Biguanides
b. Sulfonylureas
c. Thiazolidinediones
d. Alpha-glucosidase inhibitors

A

b. Sulfonylureas

120
Q

Which sulfonylurea is recommended as a safer alternative during pregnancy?
a. Glipizide
b. Glimepiride
c. Tolbutamide
d. Glyburide

A

d. Glyburide

121
Q

Which of the following is an adverse effect of sulfonylureas?
a. Weight gain
b. Weight loss
c. Hyperglycemia
d. Hyperkalemia

A

a. Weight gain

122
Q

Sulfonylureas can cause which serious side effect due to excessive insulin release?
a. Hyperglycemia
b. Hypoglycemia
c. Hypertension
d. Hyperlipidemia

A

b. Hypoglycemia

123
Q

Renal impairment is a particular problem in agents metabolized to:
a. Inactive compounds
b. Active compounds
c. Neutral compounds
d. Soluble compounds

A

b. Active compounds

124
Q

Which sulfonylurea is particularly problematic in patients with renal impairment?
a. Glipizide
b. Glimepiride
c. Glyburide
d. Tolbutamide

A

c. Glyburide

125
Q

What is a common adverse effect of sulfonylureas related to insulin action?
a. Increased blood pressure
b. Weight gain
c. Reduced appetite
d. Dehydration

A

b. Weight gain

126
Q

Sulfonylureas are known to cause hypoglycemia due to their effect on:
a. Decreasing insulin secretion
b. Increasing insulin release
c. Reducing insulin sensitivity
d. Inhibiting glucose absorption

A

b. Increasing insulin release

127
Q

Patients with renal impairment should be cautious with sulfonylureas that are:
a. Excreted unchanged
b. Metabolized to inactive compounds
c. Metabolized to active compounds
d. Highly protein-bound

A

c. Metabolized to active compounds

128
Q

Which of the following is a less common adverse effect of sulfonylureas?
a. Weight gain
b. Hypoglycemia
c. Hyperglycemia
d. Renal impairment

A

c. Hyperglycemia

129
Q

The action of meglitinide analogs is dependent on:
a. Liver function
b. Functioning pancreatic β cells
c. Kidney function
d. Muscle cells

A

b. Functioning pancreatic β cells

130
Q

Meglitinide analogs bind to a distinct site on which receptor?
a. Sulfonylurea receptor of ATP-sensitive K+ channels
b. Insulin receptor
c. Glucagon receptor
d. GLUT4 receptor

A

a. Sulfonylurea receptor of ATP-sensitive K+ channels

131
Q

The mechanism of action of meglitinide analogs is similar to which other class of drugs?
a. Biguanides
b. Thiazolidinediones
c. Sulfonylureas
d. Alpha-glucosidase inhibitors

A

c. Sulfonylureas

132
Q

Meglitinide analogs have a rapid onset and a:
a. Long duration of action
b. Variable duration of action
c. Short duration of action
d. Intermediate duration of action

A

c. Short duration of action

133
Q

Meglitinide analogs are effective in the early release of insulin that occurs:
a. Before bedtime
b. After a meal
c. In the morning
d. During exercise

A

b. After a meal

134
Q

Meglitinide analogs are primarily used as:
a. Fasting glucose regulators
b. Postprandial glucose regulators
c. Long-term glucose regulators
d. Insulin sensitizers

A

b. Postprandial glucose regulators

135
Q

The primary effect of meglitinide analogs is achieved by:
a. Stimulating insulin release
b. Inhibiting glucose absorption
c. Enhancing glucose uptake
d. Reducing hepatic glucose production

A

a. Stimulating insulin release

136
Q

Which of the following best describes the duration of action of meglitinide analogs compared to sulfonylureas?
a. Longer
b. Shorter
c. The same
d. Variable

A

b. Shorter

137
Q

Compared to sulfonylureas, the incidence of hypoglycemia with meglitinides is:
a. Lower
b. Higher
c. The same
d. Variable

A

a. Lower

138
Q

Why should meglitinides not be used in combination with sulfonylureas?
a. They decrease insulin sensitivity
b. They increase glucose absorption
c. They cause severe hypoglycemia
d. They reduce the effectiveness of insulin

A

c. They cause severe hypoglycemia

139
Q

Which of the following drugs is a meglitinide analog?
a. Repaglinide
b. Glyburide
c. Glipizide
d. Glimepiride

A

a. Repaglinide

140
Q

Which of the following is also a meglitinide analog?
a. Glimepiride
b. Glipizide
c. Nateglinide
d. Glyburide

A

c. Nateglinide

141
Q

Meglitinides should be avoided in combination with which class of drugs to prevent severe hypoglycemia?
a. Sulfonylureas
b. Biguanides
c. Thiazolidinediones
d. Alpha-glucosidase inhibitors

A

a. Sulfonylureas

142
Q

Which meglitinide is included in this class of agents?
a. Glyburide
b. Repaglinide
c. Glipizide
d. Glimepiride

A

b. Repaglinide

143
Q

The primary function of meglitinides is to:
a. Reduce glucose absorption
b. Increase hepatic glucose production
c. Stimulate insulin release
d. Inhibit insulin release

A

c. Stimulate insulin release

144
Q

What is the benefit of using meglitinides over sulfonylureas?
a. Lower risk of hypoglycemia
b. Longer duration of action
c. Higher potency
d. Reduced side effects

A

a. Lower risk of hypoglycemia

145
Q

Which of the following drugs inhibits CYP3A4 and may enhance the effect of repaglinide?
a. Ketoconazole
b. Rifampin
c. Carbamazepine
d. Barbiturates

A

a. Ketoconazole

146
Q

Why must drugs that inhibit CYP3A4 be used with caution in hepatic impairment when taken with repaglinide?
a. They decrease the effect of repaglinide
b. They enhance the effect of repaglinide
c. They have no effect on repaglinide
d. They increase the clearance of repaglinide

A

b. They enhance the effect of repaglinide

147
Q

Which of the following is a CYP3A4 inducer that decreases the effect of repaglinide?
a. Barbiturates
b. Ketoconazole
c. Erythromycin
d. Clarithromycin

A

a. Barbiturates

148
Q

Which of the following is an effect of CYP3A4 inducers on repaglinide?
a. Enhance the effect
b. Decrease the effect
c. No effect
d. Variable effect

A

b. Decrease the effect

149
Q

What is the impact of weight gain with meglitinides compared to sulfonylureas?
a. It is less problematic
b. It is more problematic
c. It is equally problematic
d. It does not occur

A

a. It is less problematic

150
Q

Patients with hepatic impairment should use caution when taking repaglinide with which type of drugs?
a. CYP3A4 inducers
b. CYP3A4 inhibitors
c. Antihypertensives
d. Antihistamines

A

b. CYP3A4 inhibitors

151
Q

Which antibiotic may enhance the effect of repaglinide by inhibiting CYP3A4?
a. Rifampin
b. Carbamazepine
c. Erythromycin
d. Barbiturates

A

c. Erythromycin

152
Q

Compared to sulfonylureas, meglitinides are associated with:
a. Less weight gain
b. More weight gain
c. No weight gain
d. Similar weight gain

A

a. Less weight gain

153
Q

The only drug member of the biguanides class is:
a. Metformin
b. Glyburide
c. Repaglinide
d. Pioglitazone

A

a. Metformin

154
Q

Metformin increases glucose uptake by target tissues, thereby:
a. Increasing insulin secretion
b. Enhancing gluconeogenesis
c. Decreasing insulin resistance
d. Reducing insulin sensitivity

A

c. Decreasing insulin resistance

155
Q

For its action, metformin requires:
a. Glucagon
b. Adrenaline
c. Insulin
d. Somatostatin

A

c. Insulin

156
Q

Which of the following is NOT a main mechanism of action of metformin?
a. Inhibiting hepatic gluconeogenesis
b. Promoting insulin secretion
c. Slowing intestinal absorption of sugars
d. Improving peripheral glucose uptake and utilization

A

b. Promoting insulin secretion

157
Q

Metformin’s effects on lipid profiles include:
a. Increasing LDL and VLDL
b. Decreasing HDL
c. Reducing LDL, VLDL, and increasing HDL
d. Increasing triglycerides

A

c. Reducing LDL, VLDL, and increasing HDL

158
Q

How long do the lipid profile effects of metformin typically take to manifest?
a. 1-2 weeks
b. 4-6 weeks
c. 8-10 weeks
d. 10-12 weeks

A

b. 4-6 weeks

159
Q

Metformin often causes weight loss due to:
a. Loss of appetite
b. Increased energy expenditure
c. Enhanced fat oxidation
d. Decreased carbohydrate intake

A

a. Loss of appetite

160
Q

Which of the following is true regarding metformin and insulin secretion?
a. Metformin increases insulin secretion
b. Metformin does not promote insulin secretion
c. Metformin decreases insulin secretion
d. Metformin has no effect on insulin secretion

A

b. Metformin does not promote insulin secretion

161
Q

Metformin is recommended as the drug of choice for which condition?
a. Type 2 diabetes
b. Type 1 diabetes
c. Gestational diabetes
d. Insulinoma

A

a. Type 2 diabetes

162
Q

How is metformin primarily excreted from the body?
a. Metabolized by the liver
b. Excreted unchanged in bile
c. Excreted unchanged renally
d. Metabolized by the kidneys

A

c. Excreted unchanged renally

163
Q

Metformin is not metabolized in which organ?
a. Kidneys
b. Liver
c. Lungs
d. Pancreas

A

b. Liver

164
Q

Metformin is effective in the treatment of polycystic ovary disease (PCOD) because it:
a. Increases insulin secretion
b. Reduces appetite
c. Increases estrogen levels
d. Lowers insulin resistance

A

d. Lowers insulin resistance

165
Q

The ability of metformin to lower insulin resistance in women with PCOD can result in:
a. Decreased testosterone levels
b. Increased prolactin levels
c. Ovulation and possibly pregnancy
d. Reduced menstrual bleeding

A

c. Ovulation and possibly pregnancy

166
Q

Which statement is true regarding metformin and insulin secretion?
a. Metformin promotes insulin secretion
b. Metformin does not promote insulin secretion
c. Metformin decreases insulin secretion
d. Metformin enhances insulin degradation

A

b. Metformin does not promote insulin secretion

167
Q

Which of the following is a common adverse effect of metformin?
a. Hypoglycemia
b. Weight gain
c. Gastrointestinal disturbance
d. Hyperkalemia

A

c. Gastrointestinal disturbance

168
Q

Metformin is contraindicated in patients with which conditions?
a. Hypertension and asthma
b. Renal and hepatic disease
c. Hyperlipidemia and gout
d. Osteoporosis and anemia

A

b. Renal and hepatic disease

169
Q

Why is metformin contraindicated in renal and hepatic disease?
a. It increases insulin resistance
b. It increases the risk of lactic acidosis
c. It reduces glucose uptake
d. It promotes gluconeogenesis

A

b. It increases the risk of lactic acidosis

170
Q

Which of the following conditions is a contraindication for metformin use?
a. Acute myocardial infarction and congestive heart failure
b. Hyperthyroidism and Addison’s disease
c. Rheumatoid arthritis and lupus
d. Osteoarthritis and chronic bronchitis

A

a. Acute myocardial infarction and congestive heart failure

171
Q

Metformin is contraindicated in patients with:
a. Mild infections
b. Severe infection
c. Chronic allergies
d. Seasonal flu

A

b. Severe infection

172
Q

Metformin use is contraindicated in diabetic ketoacidosis because:
a. It may exacerbate lactic acidosis
b. It promotes insulin resistance
c. It decreases insulin secretion
d. It increases glucose absorption

A

a. It may exacerbate lactic acidosis

173
Q

Long-term use of metformin may interfere with the absorption of:
a. Vitamin D
b. Vitamin B12
c. Vitamin K
d. Vitamin C

A

b. Vitamin B12

174
Q

Why is hypoglycemia less common with metformin than with sulfonylureas?
a. Metformin does not promote insulin secretion
b. Metformin increases insulin secretion
c. Metformin decreases glucose absorption
d. Metformin enhances gluconeogenesis

A

a. Metformin does not promote insulin secretion

175
Q

Which of the following drugs is a member of the thiazolidinedione class?
a. Pioglitazone
b. Metformin
c. Glyburide
d. Repaglinide

A

a. Pioglitazone

176
Q

Which drug is included in the thiazolidinedione class?
a. Glipizide
b. Metformin
c. Rosiglitazone
d. Nateglinide

A

c. Rosiglitazone

177
Q

What is the primary mechanism of action for thiazolidinediones?
a. They target the peroxisome proliferator-activated receptor (PPARγ)
b. They increase insulin secretion from beta cells
c. They inhibit hepatic gluconeogenesis
d. They decrease glucose absorption in the intestines

A

a. They target the peroxisome proliferator-activated receptor (PPARγ)

178
Q

Thiazolidinediones regulate which of the following in the body?
a. Protein synthesis
b. Amino acid metabolism
c. Fat and glucose metabolism
d. Electrolyte balance

A

c. Fat and glucose metabolism

179
Q

Increased insulin sensitivity in which tissues is a result of thiazolidinedione action?
a. Brain and heart
b. Skin and kidneys
c. Adipose tissue, liver, and skeletal muscle
d. Bone and cartilage

A

c. Adipose tissue, liver, and skeletal muscle

180
Q

The action of thiazolidinediones involves regulation of which receptor?
a. Insulin receptor
b. Glucagon receptor
c. Dopamine receptor
d. Peroxisome proliferator-activated receptor (PPARγ)

A

d. Peroxisome proliferator-activated receptor (PPARγ)

181
Q

Thiazolidinediones do not promote which of the following?
a. Glucose uptake
b. Insulin secretion
c. Insulin sensitivity
d. Fat metabolism

A

b. Insulin secretion

182
Q

Which of the following drugs does not affect LDL levels?
a. Pioglitazone
b. Rosiglitazone
c. Metformin
d. Glyburide

A

a. Pioglitazone

183
Q

Rosiglitazone has been associated with an increase in which of the following?
a. HDL and LDL
b. LDL
c. Triglycerides
d. Total cholesterol

A

b. LDL

184
Q

Both pioglitazone and rosiglitazone have what effect on HDL levels?
a. Increase HDL levels
b. Decrease HDL levels
c. No effect on HDL levels
d. Decrease LDL levels

A

a. Increase HDL levels

185
Q

Thiazolidinediones (TZDs) lead to redistribution of fat from visceral to subcutaneous tissues, resulting in:
a. Weight loss
b. Weight gain
c. Muscle gain
d. Fat loss

A

b. Weight gain

186
Q

The cardiovascular toxicity and water retention associated with which drug can lead to an increase in LDL levels?
a. Pioglitazone
b. Rosiglitazone
c. Metformin
d. Glimepiride

A

b. Rosiglitazone

187
Q

Which of the following is not affected by pioglitazone?
a. HDL
b. VLDL
c. Total cholesterol
d. LDL

A

d. LDL

188
Q

Which drug increases LDL levels?
a. Pioglitazone
b. Rosiglitazone
c. Metformin
d. Insulin

A

b. Rosiglitazone

189
Q

What is a common effect of both pioglitazone and rosiglitazone on HDL?
a. Increase in HDL levels
b. Decrease in HDL levels
c. No effect on HDL levels
d. Variable effect on HDL levels

A

a. Increase in HDL levels

190
Q

What is one of the potential adverse effects of rosiglitazone due to increased LDL?
a. Hyperglycemia
b. Cardiovascular toxicity
c. Hypotension
d. Anemia

A

b. Cardiovascular toxicity

191
Q

Thiazolidinediones lead to the redistribution of fat from visceral to subcutaneous tissues, causing what side effect?
a. Hypertension
b. Hypoglycemia
c. Weight gain
d. Osteoporosis

A

c. Weight gain

192
Q

Glitazones are recommended as a second-line alternative for patients who fail or have contraindications to which therapy?
a. Insulin
b. Metformin
c. Sulfonylureas
d. DPP-4 inhibitors

A

b. Metformin

193
Q

How are glitazones absorbed in the body?
a. Poorly from the GIT
b. Well from the GIT
c. Only in the presence of food
d. Only when injected

A

b. Well from the GIT

194
Q

Which of the following statements is true about glitazones in nursing mothers?
a. Recommended for use
b. Not recommended for use
c. No known effects
d. Required in high doses

A

b. Not recommended for use

195
Q

Relief of insulin resistance by glitazones can cause ovulation to resume in which group of women?
a. Postmenopausal women
b. Pregnant women
c. Premenopausal women with polycystic ovary syndrome
d. All women

A

c. Premenopausal women with polycystic ovary syndrome

196
Q

Why might women taking oral contraceptives and TZDs become pregnant?
a. TZDs reduce plasma concentrations of estrogen-containing contraceptives
b. TZDs increase estrogen levels
c. TZDs decrease contraceptive absorption
d. TZDs have no effect on contraceptives

A

a. TZDs reduce plasma concentrations of estrogen-containing contraceptives

197
Q

Which of the following is not an adverse effect of glitazones?
a. Hyperglycemia
b. Weight increase
c. Osteopenia and increased fracture risk
d. Increased risk of myocardial infarction and death

A

a. Hyperglycemia

198
Q

Which of the following adverse effects of glitazones occurs very rarely?
a. Osteopenia
b. Weight increase
c. Liver toxicity
d. Increased fracture risk

A

c. Liver toxicity

199
Q

Which of the following is an alpha-glucosidase inhibitor?
a. Acarbose
b. Metformin
c. Insulin
d. Glipizide

A

a. Acarbose

200
Q

Alpha-glucosidase inhibitors are used for the treatment of which condition?
a. Type 2 diabetes
b. Hypertension
c. Hyperlipidemia
d. Type 1 diabetes

A

a. Type 2 diabetes

201
Q

When should alpha-glucosidase inhibitors be taken?
a. After meals
b. At the beginning of meals
c. Before bed
d. On an empty stomach

A

b. At the beginning of meals

202
Q

How do alpha-glucosidase inhibitors work?
a. By increasing insulin secretion
b. By delaying the digestion of carbohydrates
c. By increasing glucose absorption
d. By decreasing insulin resistance

A

b. By delaying the digestion of carbohydrates

203
Q

What is the mechanism of action of alpha-glucosidase inhibitors?
a. Reversibly inhibiting alpha-glucosidase in the intestinal brush border
b. Irreversibly inhibiting alpha-glucosidase in the liver
c. Increasing pancreatic beta-cell activity
d. Enhancing insulin receptor sensitivity

A

a. Reversibly inhibiting alpha-glucosidase in the intestinal brush border

204
Q

Which enzyme do alpha-glucosidase inhibitors inhibit in the pancreas?
a. Lipase
b. Trypsin
c. Alpha-amylase
d. Pepsin

A

c. Alpha-amylase

205
Q

Which alpha-glucosidase inhibitor is poorly absorbed?
a. Acarbose
b. Miglitol
c. Metformin
d. Glipizide

A

a. Acarbose

206
Q

Which alpha-glucosidase inhibitor is very well absorbed but has no systemic effects?
a. Acarbose
b. Miglitol
c. Metformin
d. Glipizide

A

b. Miglitol

207
Q

What are the major side effects of alpha-glucosidase inhibitors?
a. Hypoglycemia and weight gain
b. Flatulence, diarrhea, and abdominal cramping
c. Hypertension and tachycardia
d. Nausea and vomiting

A

b. Flatulence, diarrhea, and abdominal cramping

208
Q

Why should patients with inflammatory bowel disease avoid alpha-glucosidase inhibitors?
a. They can worsen colonic ulceration or intestinal obstruction
b. They cause systemic toxicity
c. They increase blood glucose levels
d. They cause severe hypoglycemia

A

a. They can worsen colonic ulceration or intestinal obstruction

209
Q

Sitagliptin inhibits which enzyme?
a. DPP-IV
b. Alpha-amylase
c. Alpha-glucosidase
d. Pepsin

A

a. DPP-IV

210
Q

What is the role of DPP-IV?
a. Enhances insulin secretion
b. Inactivates incretin hormones such as GLP-1
c. Increases glucose absorption
d. Decreases glucagon secretion

A

b. Inactivates incretin hormones such as GLP-1

211
Q

How does sitagliptin affect incretin hormones?
a. Prevents incretin hormone inactivation
b. Decreases incretin hormone levels
c. Increases glucagon levels
d. Enhances insulin resistance

A

a. Prevents incretin hormone inactivation

212
Q

Which of the following is a result of sitagliptin preventing incretin hormone inactivation?
a. Increased insulin release in response to meals
b. Decreased insulin release in response to meals
c. Increased inappropriate secretion of glucagon
d. Decreased insulin sensitivity

A

a. Increased insulin release in response to meals

213
Q

Sitagliptin is well absorbed after which type of administration?
a. Oral administration
b. Intravenous administration
c. Subcutaneous administration
d. Intramuscular administration

A

a. Oral administration

214
Q

How is the majority of sitagliptin excreted from the body?
a. Through feces
b. Unchanged in the urine
c. Metabolized in the liver
d. Through sweat

A

b. Unchanged in the urine

215
Q

Dosage adjustments of sitagliptin are recommended for patients with which condition?
a. Renal dysfunction
b. Hepatic dysfunction
c. Cardiac dysfunction
d. Pulmonary dysfunction

A

a. Renal dysfunction

216
Q

What are the most common adverse effects of sitagliptin?
a. Nasopharyngitis and headache
b. Hypoglycemia and weight gain
c. Hypertension and tachycardia
d. Nausea and vomiting

A

a. Nasopharyngitis and headache

217
Q

The rate of hypoglycemia with sitagliptin is:
a. Very low
b. Moderate
c. High
d. Unpredictable

A

a. Very low

218
Q

What is the incretin effect?
a. Increased glucagon secretion with intravenous glucose
b. Higher secretion of insulin with oral glucose compared to intravenous glucose
c. Lower secretion of insulin with oral glucose compared to intravenous glucose
d. Increased glucose absorption in the intestines

A

b. Higher secretion of insulin with oral glucose compared to intravenous glucose

219
Q

Incretin effect is reduced in which condition?
a. Type 1 diabetes
b. Type 2 diabetes
c. Hypertension
d. Hyperlipidemia

A

b. Type 2 diabetes

220
Q

Which of the following is an incretin mimetic?
a. Exenatide
b. Metformin
c. Sitagliptin
d. Insulin

A

a. Exenatide

221
Q

What does exenatide improve?
a. Glucose-dependent insulin secretion
b. Insulin resistance
c. Glucagon secretion
d. Glucose absorption

A

a. Glucose-dependent insulin secretion

222
Q

Which effect is NOT associated with exenatide?
a. Slows gastric emptying time
b. Decreases food intake
c. Increases postprandial glucagon secretion
d. Promotes beta-cell proliferation

A

c. Increases postprandial glucagon secretion

223
Q

What are the consequences of exenatide administration?
a. Weight gain and increased HbA1c
b. Weight loss and reduced postprandial hyperglycemia
c. Increased insulin resistance
d. Increased glucose absorption

A

b. Weight loss and reduced postprandial hyperglycemia

224
Q

How should exenatide be administered?
a. Orally before meals
b. Subcutaneously before meals
c. Intramuscularly after meals
d. Intravenously during meals

A

b. Subcutaneously before meals

225
Q

What are the main adverse effects of exenatide?
a. Hypoglycemia and weight gain
b. Nausea, vomiting, and diarrhea
c. Hypertension and tachycardia
d. Nausea and headache

A

b. Nausea, vomiting, and diarrhea

226
Q

Which of the following drugs is an SGLT2 inhibitor?
a. Canagliflozin
b. Metformin
c. Sitagliptin
d. Insulin

A

a. Canagliflozin

227
Q

SGLT2 inhibitors are used for the treatment of which condition?
a. Hypertension
b. Type 2 diabetes
c. Type 1 diabetes
d. Hyperlipidemia

A

b. Type 2 diabetes

228
Q

What is the mechanism of action of SGLT2 inhibitors?
a. Increasing insulin secretion
b. Decreasing glucagon secretion
c. Decreasing reabsorption of glucose in the kidney
d. Increasing glucose absorption in the intestines

A

c. Decreasing reabsorption of glucose in the kidney

229
Q

What is the effect of inhibiting SGLT2 in the kidneys?
a. Increased blood glucose
b. Increased urinary glucose excretion
c. Decreased urinary glucose excretion
d. Increased insulin resistance

A

b. Increased urinary glucose excretion

230
Q

Which adverse effect is most commonly associated with SGLT2 inhibitors?
a. Hypoglycemia
b. Weight gain
c. Female genital mycotic infections
d. Hypertension

A

c. Female genital mycotic infections

231
Q

Why are SGLT2 inhibitors not indicated for the treatment of hypertension?
a. They increase blood pressure
b. They have no effect on blood pressure
c. They are primarily indicated for glucose control
d. They cause severe hypotension

A

c. They are primarily indicated for glucose control

232
Q

What is an additional effect of inhibiting SGLT2?
a. Increased insulin sensitivity
b. Decreased reabsorption of sodium
c. Increased reabsorption of potassium
d. Decreased glucagon secretion

A

b. Decreased reabsorption of sodium

233
Q

What is the second most common adverse effect of SGLT2 inhibitors?
a. Hypoglycemia
b. Urinary tract infections
c. Diarrhea
d. Nausea

A

b. Urinary tract infections

Pharma2 MCQs (6 decks)

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